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[Effect of Qingshen Granules on inflammation/hepcidin axis and iron metabolism in patients with renal anemia: a single-center, randomized controlled trial].
Zhang, L, Wang, Y, Jin, H, Wang, D, Wei, L, Ren, K, Mao, Y
Nan fang yi ke da xue xue bao = Journal of Southern Medical University. 2019;(10):1155-1159
Abstract
OBJECTIVE To evaluate the therapeutic effect of Qingshen Granules on renal anemia in patients with damp-heat syndrome and explore the mechanisms in light of inflammation/hepcidin axis and iron metabolism. METHODS Sixty patients with renal anemia and dampness-heat syndrome were randomized into control group (n=30) and treatment group (n=30). All the patients were given routine treatment, and the patients in the treatment group received additional treatment with Qingshen Granules (3 times a day). After 12 weeks of treatments, the patients were examined for changes in the integral value of TCM syndrome, serum creatinine (Scr), glomerular filtration rate (eGFR), hemoglobin (HGB), hematocrit (HCT), red blood cell (RBC) count, interleukin-6 (IL-6), hypersensitive C-reactive protein (hs-CRP), ferritin, growth differentiation factor-15 (GDF-15), serum iron (SI), total iron binding capacity (TIBC), transferrin saturation (TAST), soluble transferrin receptor (sTfR) and ferritin levels. RESULTS After the treatment, the scores of TCM syndrome were significantly improved in the treatment group and were better than those in the control group (P=0.000). Scr and eGFR were improved in both groups after the treatment. The levels of HGB, HCT and RBC were all improved in the two groups after treatment, and the improvements were more obvious in the treatment group (P=0.002, 0.002, and 0.017, respectively). The levels of IL-6, hs-CRP, hepcidine and GDF-15 were all lowered in the two groups after the treatment, and they were all significantly lower in the treatment group than in the control group (all P=0.000). The treatments increased the levels of SI and TAST in both of the groups, and compared with those in control group, the levels of TIBC, sTfR and ferritin were significantly lowered in the treatment group after the 12-week treatment (P=0.000). CONCLUSIONS Qingshen granules can effectively improve renal anemia in patients with damp-heat syndrome possibly by improving iron metabolism through alleviation of inflammation and reduction of hepcidine level.
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Iron overload in congenital haemolytic anaemias: role of hepcidin and cytokines and predictive value of ferritin and transferrin saturation.
Barcellini, W, Zaninoni, A, Gregorini, AI, Soverini, G, Duca, L, Fattizzo, B, Giannotta, JA, Pedrotti, P, Vercellati, C, Marcello, AP, et al
British journal of haematology. 2019;(3):523-531
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Abstract
Iron overload (IO) is poorly investigated in the congenital haemolytic anaemias (CHAs), a heterogeneous group of rare inherited diseases encompassing abnormalities of the erythrocyte membrane and metabolism, and defects of the erythropoiesis. In this study we systematically evaluated routine iron parameters and cardiac and hepatic magnetic resonance imaging, together with erythropoietin, hepcidin, non-transferrin bound iron (NTBI), and cytokine serum levels in patients with different CHAs. We found that 40% of patients had a liver iron concentration (LIC) >4 mg Fe/g dry weight. Hepatic IO was associated with ferritin levels (P = 0·0025), transferrin saturation (TfSat, P = 0·002) and NTBI (P = 0·003). Moreover, ferritin >500 μg/l plus TfSat >60% was demonstrated as the best combination able to identify increased LIC, and TfSat alteration as more important in cases with discordant values. Possible confounding factors, such as transfusions, hepatic disease, metabolic syndrome and hereditary haemochromatosis-associated mutations, had negligible effects on IO. Erythropoietin and hepcidin levels were increased in CHAs compared with controls, correlating with LIC and ferritin, respectively. Regarding cytokines, γ-interferon (IFN-γ) was increased, and both interleukin 6 and IFN-γ levels positively correlated with ferritin and hepcidin levels. Overall, these findings suggest the existence of a vicious cycle between chronic haemolysis, inflammatory response and IO in CHAs.
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The correlation between the concentration of hepcidin in serum and the occurrence of insulin resistance and hyperandrogenemia in women with polycystic ovary syndrome.
Pluta, D, Franik, G, Blukacz, Ł, Kowalczyk, K, Witkowska, A, Wysocka, M, Madej, P
European review for medical and pharmacological sciences. 2018;(21):7379-7384
Abstract
OBJECTIVE Scarce clinical and experimental studies suggest that hepcidin can be a protein participating in the development of metabolic disorders, while its synthesis and concentration in the circulation outside of the iron metabolism parameters can be influenced by hormones. The aim of the present study was to determine the correlation between the concentration of hepcidin in serum and the occurrence of insulin resistance and hyperandrogenemia in women with PCOS. PATIENTS AND METHODS Five groups of women with PCOS were divided based on: correct body mass (17 without hyperandrogenemia and insulin resistance - G1; 17 with hyperandrogenemia and without insulin resistance - G2; 11 without hyperandrogenemia and with insulin resistance - G3; 10 with hyperandrogenemia and insulin resistance - G4), metabolic and hormonal parameters and selected markers of iron metabolism. RESULTS Serum glucose levels were significantly higher in the group G3 than G1 and in the group G4 than G1 and G2. Serum insulin levels and HOMA-IR values were significantly higher in the groups G3 and G4 than G1 and G2. Serum androstenedione levels were significantly higher in the group G2 than G1 and G3 than G2. Serum transferrin levels were significantly lower in the group G1 than in the reaming study groups. CONCLUSIONS It has been demonstrated that insulin resistance and hyperandrogenemia appear to be the factors decreasing the concentration of transferrin circulation, but not the remaining parameters of the iron metabolism in the studied women. No relationship between the concentration of hepcidin circulation and other studied parameters of the iron metabolism and the parameters of the carbohydrate metabolism was discovered. Androstenedione can stimulate hepcidin synthesis in women with PCOS with correct body mass.
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[ANEMIC SYNDROME IN PATIENTS WITH COMMUNITY-ACQUIRED PNEUMONIA].
Budnevsky, AV, Esaulenko, IE, Ovsyannikov, ES, Labzhaniya, NB, Voronina, EV, Chernov, AV
Klinicheskaia meditsina. 2016;(1):56-60
Abstract
Community-acquired pneumonia remains a most widespread acute infectious disease of socio-economic significance all over the world. Up to 30% of the patients present with anemia responsible for the unfavourable prognosis and elevated mortality. Not infrequently, anemia is not diagnosed during the hospital stay und therefore remains uncorrected. Severe anemia results in enhanced hypercapnia and slowed maturation of red blood cells in the bone marrow which facilitates the development of ischemic syndrome. Hepcidin, a mediator of inflammation and iron-regulatory hormone, plays an important role in the clinical course of community-acquired pneumonia. Hepsidin production increases during inflammation; it suppresses erythtropoiesis and depletes the iron depot leading to so-called anemia of inflammation. Hypoxia and anemia activate erythtropoiesis, and the released erythropoietin inhibits hepsidin production. During pneumonia resolution, hepsidin promotes recovery from anemia by activating iron absorption. The curreni literature contains few data on the use of hepcidin as a diagnostic marker of anemia. The necessity oftreating anemia in patients with pneumonia under hospital conditions is a matter of discussion. Direct involvement of hepcidin in iron metabolism creates a prerequisite for the treatment of anemia. Medicamental suppression of its activity by stimulating erythtropoiesis can facilitate normalization of iron metabolism and restoration of hemoglobin level.
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Iron and the liver.
Pietrangelo, A
Liver international : official journal of the International Association for the Study of the Liver. 2016;:116-23
Abstract
Humans have evolved to retain iron in the body and are exposed to a high risk of iron overload and iron-related toxicity. Excess iron in the blood, in the absence of increased erythropoietic needs, can saturate the buffering capacity of serum transferrin and result in non-transferrin-bound highly reactive forms of iron that can cause damage, as well as promote fibrogenesis and carcinogenesis in the parenchymatous organs. A number of hereditary or acquired diseases are associated with systemic or local iron deposition or iron misdistribution in organs or cells. Two of these, the HFE- and non-HFE hemochromatosis syndromes represent the paradigms of genetic iron overload. They share common clinical features and the same pathogenic basis, in particular, a lack of synthesis or activity of hepcidin, the iron hormone. Before hepcidin was discovered, the liver was simply regarded as the main site of iron storage and, as such, the main target of iron toxicity. Now, as the main source of hepcidin, it appears that the loss of the hepcidin-producing liver mass or genetic and acquired factors that repress hepcidin synthesis in the liver may also lead to iron overload. Usually, there is low-grade excess iron which, through oxidative stress, is sufficient to worsen the course of the underlying liver disease or other chronic diseases that are apparently unrelated to iron, such as chronic metabolic and cardiovascular diseases. In the future, modulation of hepcidin synthesis and activity or hepcidin hormone-replacing strategies may become therapeutic options to cure iron-related disorders.
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[Anemic syndrome in rheumatoid arthritis: Diagnostic approaches and treatment opportunities].
Grinshtein, YI, Shabalin, VV, Kusaev, VV
Terapevticheskii arkhiv. 2016;(5):107-112
Abstract
Anemia of chronic disease (ACD) is a leading cause of anemic syndrome in patients with rheumatoid arthritis (RA). Enhanced hepcidin production mainly stimulated by excess interleukin-6 levels is a key pathodgentic component of ACD (frequently known as anemia of inflammation) by causing the degradation of the transmembrane protein ferroportin, hepcidin impairs iron metabolism. On the basis of the material of recent publications the review gives present-day views on the pathodgenesis of ACD in RA, approaches to the diagnosis and differential diagnosis of ACD, especially in its concomitance with iron-deficiency anemia, as well as approaches to therapy for the type of anemic syndrome with the complex mechanism for its development.
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Genetics, Genetic Testing, and Management of Hemochromatosis: 15 Years Since Hepcidin.
Pietrangelo, A
Gastroenterology. 2015;(5):1240-1251.e4
Abstract
The discovery of hepcidin in 2000 and the subsequent unprecedented explosion of research and discoveries in the iron field have dramatically changed our understanding of human disorders of iron metabolism. Today, hereditary hemochromatosis, the paradigmatic iron-loading disorder, is recognized as an endocrine disease due to the genetic loss of hepcidin, the iron hormone produced by the liver. This syndrome is due to unchecked transfer of iron into the bloodstream in the absence of increased erythropoietic needs and its toxic effects in parenchymatous organs. It is caused by mutations that affect any of the proteins that help hepcidin to monitor serum iron, including HFE and, in rarer instances, transferrin-receptor 2 and hemojuvelin, or make its receptor ferroportin, resistant to the hormone. In Caucasians, C282Y HFE homozygotes are numerous, but they are only predisposed to hemochromatosis; complete organ disease develops in a minority, due to alcohol abuse or concurrent genetic modifiers that are now being identified. HFE gene testing can be used to diagnose hemochromatosis in symptomatic patients, but analyses of liver histology and full gene sequencing are required to identify patients with rare, non-HFE forms of the disease. Due to the central pathogenic role of hepcidin, it is anticipated that nongenetic causes of hepcidin loss (eg, end-stage liver disease) can cause acquired forms of hemochromatosis. The mainstay of hemochromatosis management is still removal of iron by phlebotomy, first introduced in 1950s, but identification of hepcidin has not only shed new light on the pathogenesis of the disease and the approach to diagnosis, but etiologic therapeutic applications from these advances are now foreseen.
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[The clinical significance of hepcidin detection in the patients with anemia and rheumatoid arthritis].
Galushko, EA
Klinicheskaia meditsina. 2014;(6):21-7
Abstract
The prevalence of anemia in patients with rheumatoid arthritis (RA) varies from 30 to 70%. 25% of the cases are diagnosed within 1 year after onset of the disease. On the whole, anemia in RA is described as anemia of a chronic disease (ACD). Pathogenesis ofACD is a multifactor process underlain by an immune mechanism: cytokines and cells ofthe reticuloendothelial system cause changes in iron homeostasis, proliferation of erythroid precursors, erythropoietin production and lifespan of erythrocytes. The key pathogenetic factor is disordered iron metabolism. IL-6 increasing hepatic production acute-phase protein (hepcidin) is the most important cytokine involved in ACD pathogenesis. Hence the necessity to measure its serum level for differential diagnostics of anemic syndrome in patients with RA and the choice of effective basal therapy. Recent data on the therapeutic potency of tocilizumab (IL-6 receptor inhibitor) demonstrate not its safety and sustainable beneficial clinical effect in combination with the favourable action on hemoglobin profile and reduction offatigue.